Inhibition of Mitochondrial Respiration and Rapid Depletion of Mitochondrial Glutathione by β-Phenethyl Isothiocyanate: Mechanisms for Anti-Leukemia Activity-Reference-Cited by-同舟云学术

Inhibition of Mitochondrial Respiration and Rapid Depletion of Mitochondrial Glutathione by β-Phenethyl Isothiocyanate: Mechanisms for Anti-Leukemia Activity

Published:2011-12 Issue:12 Volume:15 Page:2911-2921
ISSN:1523-0864
Container-title:Antioxidants & Redox Signaling
language:en
Short-container-title:Antioxidants & Redox Signaling

Author:

Chen Gang¹,Chen Zhao¹,Hu Yumin²,Huang Peng¹²

Affiliation:

1. Department of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.

2. State Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, China.

Publisher

Mary Ann Liebert Inc

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry,Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry

Link

http://www.liebertpub.com/doi/pdf/10.1089/ars.2011.4170

Reference48 articles.

1. Glutathione depletion enforces the mitochondrial permeability transition and causes cell death in HL60 cells that overexpress Bcl‐2

2. Bcl-xL overexpression attenuates glutathione depletion in FL5.12 cells following interleukin-3 withdrawal

3. Energy Converting NADH: Quinone Oxidoreductase (Complex I)

4. Kinetics and Regulation of Mammalian NADH-Ubiquinone Oxidoreductase (Complex I)

5. PEITC Induces G1 Cell Cycle Arrest on HT-29 Cells Through the Activation of p38 MAPK Signaling Pathway

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